This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. This research is studying whether vitamin D, when given in the form of ergocalciferol, decreases Parathyroid Hormone [PTH] levels in patients with End Stage Renal disease [ESRD]and secondary hyperparathyroidism. PTH helps to control the amount of calcium in the bloodstream, and also helps to control calcium loss from the bone. ESRD or kidney failure, is a common problem. There were approximately 477,583 cases of ESRD in the USA in 2005, as reported by the United States Renal data system. Vitamin D deficiency is commonly seen in patients with ESRD. This occurs because the kidneys are unable to properly convert vitamin D to its active form which is needed for normal calcium absorption. This in turn leads to a low blood calcium level. Low calcium levels in the blood cause the parathyroid gland to make too much PTH in an attempt to raise the blood calcium levels back to normal. It is important to treat elevated PTH levels in ESRD patients because it not only helps to regulate the amount of calcium in the blood, but it also prevents the bone from losing calcium. Because increased PTH causes calcium loss from the bones, it can lead to decreased bone strength, bone pain, and potential bone fractures. Elevated PTH may also be associated with heart and blood vessel disease. The standard of care in patients with ESRD, is to give activated vitamin D. This can be given in several forms, which may include medications such as Hectorol or Rocaltrol. This study is examining whether adding ergocalciferol to current treatment for hyperparathyroidism is more effective than the current treatment alone. Hyperparathyroidism refers to overactivity of the parathyroid glands, which results in excessive production of PTH.